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The inflammatory macrophage response to MCMV in mice with a retroviral immunodeficiency syndrome (MAIDS)
R J Allcock1, C D Peacock, P Price
1Department of Microbiology, University of Western Australia, Nedlands, Australia.
Abstract:
We have shown that normal C57BL/6J mice are moderately resistant to infection with murine cytomegalovirus (MCMV) and that this resistance is impaired by prior infection with LP-BM5 MuLV, which causes a disease (MAIDS) similar to early HIV-induced disease. This study investigates macrophage function in MAIDS+ mice challenged with MCMV. MAIDS reduces the influx of cells into the peritoneal cavity seen in normal C57BL/6J mice 6 days after MCMV infection. The infiltrates contained cells that resembled activated macrophages, as they took up colloidal gold, expressed the macrophage marker Mac-1, had high levels of acid phosphatase activity, and were lymphocytostatic when co-cultured with activated T cells. MAIDS+ mice had a higher percentage of cells able to take up colloidal gold and higher acid phosphatase activity per cell. The cells were also more lymphocytostatic and produced higher levels of interleukin-1 and tumor necrosis factor-alpha on days 4 and 6 after MCMV infection. Hence, MAIDS enhances baseline and induced macrophage activity, but depresses infiltration into the site of inflammation.
Insights
Murine acquired immunodeficiency syndrome (MAIDS) enhances macrophage activity but impairs their infiltration into infection sites. This impacts C57BL/6J mice
Area of Science:
- Immunology
- Virology
- Pathology
Background:
- Normal C57BL/6J mice exhibit moderate resistance to murine cytomegalovirus (MCMV).
- LP-BM5 MuLV infection causes murine acquired immunodeficiency syndrome (MAIDS), a condition mimicking early HIV disease.
- MAIDS impairs the natural resistance of C57BL/6J mice to MCMV infection.
Purpose of the Study:
- To investigate macrophage function in MAIDS-positive (MAIDS+) mice following MCMV challenge.
- To understand how MAIDS affects the cellular response and macrophage activity during MCMV infection.
Main Methods:
- Mice with MAIDS were infected with MCMV.
- Cellular infiltration into the peritoneal cavity was analyzed 6 days post-infection.
- Macrophage characteristics including colloidal gold uptake, Mac-1 expression, and acid phosphatase activity were assessed.
- Lymphocytostatic activity and cytokine production (interleukin-1, tumor necrosis factor-alpha) were measured.
Main Results:
- MAIDS reduced cellular influx into the peritoneal cavity post-MCMV infection compared to normal mice.
- MAIDS+ mice showed a higher percentage of cells with enhanced colloidal gold uptake and acid phosphatase activity.
- Macrophage-like cells in MAIDS+ mice exhibited increased lymphocytostatic properties.
- Elevated levels of interleukin-1 and tumor necrosis factor-alpha were observed in MAIDS+ mice.
Conclusions:
- MAIDS enhances both baseline and induced macrophage activity.
- Despite enhanced activity, MAIDS depresses the infiltration of macrophages to the site of inflammation.
- These altered macrophage dynamics in MAIDS+ mice have significant implications for MCMV infection outcomes.